title: [The molecular bypass: an established method for revascularisation of non-operable PAD patients or merely a future vision].
abstract: Collateral vessel growth is a physiological process that is not equally pronounced in all people. After the development of a haemodynamically relevant stenosis in vascular systems, blood flow is directed through a collateral circulation to supply ischaemic tissue. This collateral circulation exists on the capillary level and by definition, is not composed of real new vessels. Postnatal vasculogenesis (true neovascularisation) occurs in the adult organism in tumour vascularisation, wound healing, in the endometrium, and in the context of chronic diseases such as rheumatoid arthritis and psoriasis. Reopening of the occluded vessel or use of artificial bypass grafts are the most attractive therapeutic approaches for treating peripheral arterial and coronary artery disease. These strategies have been exhausted in many patients; therefore augmentation of arteriogenesis can be more useful. Arteriogenesis, the promotion of natural collateral growth, is a hot topic in vascular research. Monocytes play a key role in arteriogenesis by "homing" to areas of collateral vessel growth and locally secrete multiple essential growth factors. Furthermore, stem cells of different origins, endothelial progenitor cells or mononuclear cells are currently being used to promote vessel growth. Also, the application of growth factors such as VEGF, MCP-1, GM-CSF have been already used in clinical trials. This review article describes the physiology and pathophysiology of vascular stenoses and their compensation mechanisms. The review also gives an overview of current treatment approaches and new strategies for non-operable PAD patients. The article presents the current cell and growth factor-related studies, as well as results of balloon dilatation and stent implantation or bypass surgery studies for improvement of revascularisation.
authors.affiliation: Klinik für Kardiologie, Angiologie und Pneumologie, Universitätsklinikum Magdeburg A. ö. R., Magdeburg, Deutschland.
authors.forename: J
authors.initials: J
authors.lastname: Herold
authors.affiliation: Klinik für Kardiologie, Angiologie und Pneumologie, Universitätsklinikum Magdeburg A. ö. R., Magdeburg, Deutschland.
authors.forename: S
authors.initials: S
authors.lastname: Said
authors.affiliation: Klinik für Kardiologie, Angiologie und Pneumologie, Universitätsklinikum Magdeburg A. ö. R., Magdeburg, Deutschland.
authors.forename: R
authors.initials: R
authors.lastname: Braun-Dullaeus
mesh_terms: D000800:Angioplasty, Balloon; D018932:Chemokine CCL2 / Q000235:genetics / Q000502:physiology; D003097:Collateral Circulation / Q000235:genetics* / Q000502:physiology*; D003131:Combined Modality Therapy / Q000639:trends; D066026:Endothelial Progenitor Cells / Q000502:physiology / Q000637:transplantation; D005544:Forecasting; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000235:genetics / Q000502:physiology; D006801:Humans; D009000:Monocytes / Q000502:physiology / Q000637:transplantation; D018919:Neovascularization, Physiologic / Q000235:genetics* / Q000502:physiology*; D058729:Peripheral Arterial Disease / Q000235:genetics* / Q000503:physiopathology / Q000628:therapy*; D033581:Stem Cell Transplantation; D015607:Stents; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000502:physiology
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D016178:Granulocyte-Macrophage Colony-Stimulating Factor